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"From the earliest days of food regulation, the use of alum (aluminumsulphate) in foods has been condemned. It is universally acknowledged as a
poison in all countries. If the Bureau of Chemistry had been permitted toenforce the law ... no food product in the country would have any trace of ...
any aluminum or saccarin. No soft drink would contain caffeine or hebromin;no bleached flour would be in interstate commerce. Our food and drugs would
be wholly without adulteration ... and the health of our people would be vastlyimproved and their life greatly extended."
From History of crime against the Food Laws (1929) by Dr. Wiley, the primemover behind the original Pure Food Law and Director of the FDA. He resignedin disgust in 1912 over exceptions granted to the law and lack of enforcement.
Aluminum has been exempted from tesitng for safety by the FDA under aconvoluted logic wherein it is c lassified as GRAS. (Generally Regarded AsSafe.) It has never been tested by the FDA on its safety and there are NOrestrictions whatever on the amount or use of aluminum.
There are over 2000 references in the National Library of Medicine on adverseeffects of alumium. The following were extracted to provide a small sample of the range of toxicity of aluminum.
Chemical Registry
Aluminum toxicity has been recognized in many settings where exposure is
heavy or prolonged, where renal function is limited, or where apreviouslyaccumulated bone burden is released in stress or illness. Toxicity may
include: encephalopathy (stuttering, gait dist urbance, myoclonic jerks,seizures, coma, abnormal EEG) osteomalacia or aplastic bone disease (
associated with painful spontaneous fractures, hypercalcemia, tumorouscalcinosis ) proximal myopathy, increased risk of infection, increased leftventricular mass and decreased myocardial function microcytic anemia withvery high levels, sudden death.
Aluminum is ubiquitous in our environment; it is the third most prevalentelement in the earth's crust. The gastrointestinal tract is relatively imperviousto aluminum, absorption normally being only about 2%. Aluminum is absorbedby a mechanism related to that for calcium. Gastric acidity and oral citratefavors absorption, and H2-blockers reduce absorption. As is true for severaltrace elements, transferrin is th e primary protein binder and carrier for aluminum in the plasma, where 80% is protein bound and 20% is free or
complexed to small molecules such as citrate.
Cells appear to take up aluminum from transferrin rather than from citrate.Purified preparations of ferritin from brain and liver have been found tocontain aluminum.
It is not known if ferritin has a specific binding site for aluminum. Factorsregulating the migration of aluminum across the blood ±brain barrier are notwell understood.
Serum aluminum correlates with encephalopathy; red cell aluminum correlateswith microcytic anemia, and bone aluminum correlates with aluminum bone
disease.
Basal PTH when elevated appears to protect bone and thereby favor CNStoxicity.
Other factors favoring one form of toxicity over another are not wellunderstood.
Aluminum toxicity has been reported to impair the formation and release of
parathyroid hormone. The parathyroid glands concentrate aluminum abovelevels in surrounding tissues. Treatment of aluminum toxi city in renal failure
patients often reactivates hyperparathyroidism, which to a certain extent ishelpful for bone remodeling and healing.
Distilled Water Placed in Various Containers
Distilled water was placed in metal containers and the amount of the "Metal
Can" that disolved into the distilled water was measured daily using SpecificConductance readings. You can divide the SC number by 2 to get theapproxamite amount of atoms in ppm ( mg / l ).
4 ppm of aluminum in human blood can cause it to colagulate.
Aluminum in humans is documented to Inhibit Learning. See Below ...
Aluminum neurotoxicity in preterm infants receiving intravenous -feedingsolutions.
Bishop N.J. ± Morley R. ± Day J.P. ± Lucas A.
From: N Engl J Med (1997 May 29) 336(22):1557 -61
Aluminum, a contaminant of commercial intravenous ±feeding solutions, ispotentially neurotoxic. We investigated the effect of perinatal exposure to
intravenous aluminum on the neurologic development of infants bornprematurely.
RESULTS: The 90 infants who received the standard feeding solutions had a
mean (± SD) Bayley Mental Development Index of 95 ±22, as compared with 98 ±20 for the 92 infants who received the aluminum-depleted solutions (P=0.39).
The former were significantly more likely (39 percent, vs. 17 percent of thelatter group; P=0.03) to have a Mental Development Index of less than 85,
increasing their risk of subsequent educational problems. For all 1 57 infants
without neuromotor impairment, increasing aluminum exposure wasassociated with a reduction in the Mental Development Index (P=0.03), with anadjusted loss of one point per day of intravenous feeding for infants receivingthe standard solutions. In preterm infants, prolonged intravenous feeding withsolutions containing aluminum is associated with impaired neurologicdevelopment.
Aluminum-containing emboli in infants treated with extracorporeal membraneoxygenation.
Vogler C. ± Sotelo-Avila C. ± Lagunoff D. ± Braun P. ± Schreifels J.A. ± Weber
T.
From: N Engl J Med (1988 Jul 14) 319(2):75 -9
We found fibrin thrombi or thromboemboli at autopsy in 22 of 23 infants withrespiratory failure who had been treated with venoarterial extracorporealmembrane oxygenation (ECMO). In addition, distinctive basophilic aluminum -containing emboli were found in 12 of the infants; the distribution of theseemboli was similar to that of the thromboemboli, except that an aluminum -containing embolus was found in a lung in only 1 infant. Sixteen infants hadpulmonary thrombi or thromboemboli. We also found friable aluminum -
containing concretions adhering loosely to the mixing rods of heat exchangersthat had been used to warm the blood flowing through the ECMO circ uit; suchconcretions were not present on unused mixing rods. We propose that thesealuminum-containing concretions developed as the silicone coating of theheat exchanger wore away and aluminum metal was exposed to warm,oxygenated blood and that fragments of aluminum-containing concretionsformed emboli. This hypothesis is supported by the fact that aluminum -containing emboli were generally not present in the lungs, which are bypassedby ECMO.
Sequential serum aluminum and urine aluminum: creatinine ra tio and tissue
aluminum loading in infants with fractures/rickets.
Koo W.W. ± Krug-Wispe S.K. ± Succop P. ± Bendon R. ± Kaplan L.A.
From: Pediatrics (1992 May) 89(5 Pt 1):877-81
Aluminum toxicity is associated with the development of bone disorders,
including fractures, osteopenia, and osteomalacia. Fifty -one infants with amean (± SEM) birth weight of 1007 ±34 g, gestational age of 28.5 +/ -0.3 weeks,
and serial radiographic documentation at 3, 6, 9, and 12 months for thepresence (n = 16) or absence ( n = 35) of fractures and/or rickets were studied
at the same intervals to determine the serial changes in serum aluminumconcentrations and urine aluminum-creatinine ratios. Autopsy bone samples
were used to determine the presence of tissue aluminum. One i nfant whoreceived aluminum-containing antacid had marked increase in serum
aluminum to 83 micrograms/L while urine aluminum -creatinine ratio increased
from 0.09 to a peak of 8.53. Vertebrae from three infants at autopsy (full enteralfeeding was tolerated for 37 and 41 days in two infants, respectively) showedaluminum deposition in the zone of provisional calcification and along thenewly formed trabecula.
Aluminum in parenteral solutions revisited ² again.
Klein G.L.
From: Am J Clin Nutr (1995 Mar) 61(3):449-56
It has been a dozen years since aluminum was first shown to contaminateparenteral nutrition solutions and to be a contributing factor in thepathogenesis of metabolic bone disease in parenteral nutrition patients as wellas in uremic patients. However, there are no regulations in place to effectivelyreduce aluminum contamination of various parenterally administerednutrients, drugs, and biologic products. The purpose of this review is fourfold:1.) to summarize our knowledge of the adverse effects of aluminum on boneformation and mineralization in parenteral nutrition patients; 2.) to discuss thepossible role of aluminum in the osteopenic bone disease of preterm infants;3.) to show how lack of regulations covering aluminum content of par enteralsolutions can lead to vulnerability of new groups of patients to aluminum
toxicity, the example being given here is that of burn patients
... many questions still remain unanswered, it is clear that aluminum causes amicrocytic hypoproliferative anemia and is a factor responsible for worsening
anemia in patients with end-stage renal disease.
Arch Dermatol (1984 Oct) 120(10):1318 -22
Three patients had subcutaneous nodules at the sites of previous injections of vaccine containing tetanus toxoid, showed aluminum crystals in the nodulesfrom two patients. From the evidence available, we believe that these nodulesare a complication of inoculations with aluminum-containing vaccines.
Persistent subcutaneous nodules in patients hyposensitized with aluminum -
containing allergen extracts.
Garcia-Patos V. ± Pujol R.M. ± Alomar A. ± Cistero A. ± Curell R. ± Fernandez-Figueras M.T. ± de Moragas J.M.
From: Arch Dermatol (1995 Dec) 131(12):1421-4
These lesions have been mainly attributed to a hypersensitivity reaction toaluminum hydroxide, which is used as an absorbing agent in many vaccines
and hyposensitization preparations. Patch tests with stand ard antigens andaluminum compounds and histopathologic and ultrastructural studies were
performed on 10 patients with persistent subcutaneous nodules on the upper part of their arms after injection of aluminum -adsorbed dust and/or pollen
extracts. The nodules appeared 1 month to 6.5 years after injections.
Trace metals and degenerative diseases of the skeleton.
An increase in fibrosarcomas in a biopsy population of cats in thePennsylvania area appears to be related to the increased vaccination of catsfollowing enactment of a mandatory rabies vaccination law.
The majority of fibrosarcomas arose in sites routinely used by veterinariansfor vaccination, and 42 of 198 tumors were surrounded by lymphocytes and
macrophages containing foreign material identical to that previously descri bedin postvaccinal inflammatory injection site reactions. Some of the vaccines
used have aluminum-based adjuvants, and macrophages surrounding threetumors contained aluminum oxide identified by electron probe microanalysis
and imaged by energy-filtered electron microscopy. Persistence of inflammatory and immunological reactions associated with aluminum maypredispose the cat to a derangement of its fibrous connective tissue repair response, leading to neoplasia.
Aspects of aluminum toxicity.
Hewitt C.D. ± Savory J. ± Wills M.R.
From: Clin Lab Med (1990 Jun) 10(2):403-22
Attention was first drawn to the potential role of aluminum as a toxic metalover 50 years ago, but was dismissed as a toxic agent as recently as 15 yearsago. The accumulation of aluminum, in some patients with chronic renalfailure, is associated with the development of toxic phenomena; dialysisencephalopathy, osteomalacic dialysis osteodystrophy, and an anemia.Aluminum accumulation also occurs in patients who are not on dialysis,predominantly infants and children with immature or impaired renal function.Aluminum has also been implicated as a toxic agent in the etiology of Alzheimer's disease, Guamiam amyotrophic lateral sclerosis, andparkinsonism-dementia.
Soft tissue sarcoma associated with aluminum oxide ceramic total hip
arthroplasty. A case report.
Ryu R.K. ± Bovill E.G. Jr ± Skinner H.B. ± Murray W.R.
From: Clin Orthop (1987 Mar)(216):207-12
Malignant tumors around fracture fixation implants have been reportedsporadically for many years. Recently, however, reports of sarcomatousdegeneration around a standard cemented hip arthroplasty and around cobalt -chromium-bearing hip arthroplasties raise new questions of the malignant
potential of metallic ends prostheses. Sarcomatous changes around aluminumoxide ceramics seem not to have been reported in the literature. The presentreport may be the first documented case of an aggressive soft tissue sarcomadetected 15 months after the patient had an uncemented ceramic total hiparthroplasty. If a causal relationship exists, the incidence of this phenomenonin the United States is 250 times greater than would be expected fromstatistics on soft tissue sarcoma at the hi p.
Aluminum was the only nonorganic element present in the test site tissue.This is the first report of confirmed aluminum-induced, delayed-hypersensitivity granulomas in a tattoo.
Delayed healing in full-thickness wounds treated with aluminum chloridesolution. A histologic study with evaporimetry correlation.
Wounds were treated either with 30% aluminum chloride solution or ferricsubsulfate solution or were allowed to clot with minimal pressure from a gauzepad. Delay in reepithelialization was noted histologically both in woundstreated with aluminum chloride and in those treated with ferric subsulfate
compared to controls. Presumably this delay was the result of tissue necrosiscaused by these hemostatic agents, resulting in slightly larger and less
cosmetically acceptable scars. Plots of evaporimetry data revealed a biphasicpattern of water loss during healing, with an initial rapid decline in water loss
followed by a much slower decline.
Aluminium and injection site reactions.
Culora G.A. ± Ramsay A.D. ± Theaker J.M.
From: J Clin Pathol (1996 Oct) 49(10):844-7
To alert pathologists to the spectrum of histological appearances that may beseen in injection site reactions related to aluminium, showed unusual features
not described previously. In one, there was a sclerosing lipogranuloma -likereaction with unlined cystic spaces containing crystalline material. The other
case presented as a large symptomatic subcutaneous swelling whichicroscopically showed diffuse and wide -spread involvement of the subcutis by
a lymphoid infiltrate with prominent lymphoid follicles.
CONCLUSIONS: This report highlights the changes encountered in aluminiuminjection site reactions and emphasises that the lesions have a wider range of histological appearances than described previously.
Aluminum and gallium arrest formation of cerebrospinal fluid by themechanism of OH- depletion.
AlCl3 or GaCl3 was added to artificial cerebrospinal fluid and perfused throughthe cerebral ventricles of the rat. Depending on the metal and its concentration
(1-10 mM) the pH of the perfusate ranged from 7.2 to 3.5. At 10 mM metalchloride, yielding pH 4.7 (Al) or 3.5 (Ga), formation of cerebrospinal fluid wassuppressed 100%. This mechanism may also account for the antiperspirantaction of Al salts.
Aluminum toxicity and albumin.
Kelly A.T. ± Short B.L. ± Rains T.C. ± May J.C. ± Progar J.J.
From: ASAIO Trans (1989 Jul-Sep) 35(3):674-6
During a study of priming solutions for extracorporeal membrane oxygenation(ECMO) in the intensive care nursery, it was discovered that those solutionsusing certain brands of 25% albumin contained aluminum levels within thetoxic range. When the brand was changed to a brand known to have a lower
aluminum (Al) content, a marked drop in priming solution Al levels wasmeasured.
The role of aluminium for adverse reactions and immunogenicity of diphtheria -tetanus booster vaccine.
Mark A. ± Granstrom M.
From: Acta Paediatr (1994 Feb) 83(2):159 -63
235 schoolchildren aged 10 years received either a regular, aluminium -adsorbed diphtheria-tetanus vaccine or the same vaccine in fluid form, in
order to investigate if local side effects could be diminished by exclusion of aluminium. System reactions were rare and local reactions frequent in both
groups but larger local reactions were even more pronounced in the non -adsorbed vaccine group.
Potroom palsy? Neurologic disorder in three aluminum smelter workers.
Heyer N.J.
From: Arch Intern Med (1985 Nov) 145(11):1972 -5
We studied three patients with a progressive neurologic disorder, all of whomhad worked for over 12 years in the same potroom of an aluminum sme ltingplant. All had incoordination and an intention tremor. Two of the three patients
had cognitive deficits, and the most severely affected patient also had spasticparaparesis. None had involvement of the peripheral nervous system. Despite
extensive evaluations, the cause of these patients' problems remains obscure.
Neurotoxic effects of aluminum in animals are directed at the central nervoussystem, and theoretically long-term low-level exposure to aluminum in the
potroom could explain the findings in our patients.
Reducing aluminum: an occupation possibly associated with bladder cancer
Theriault G. ± De Guire L. ± Cordier S.
From: Can Med Assoc J (1981) 124(4):419 -422,425
These findings suggest that employment in an aluminum reduction plantaccounts for part of the excess of bladder cancer in the region studied.
(Author abstract) (85 Refs)
Immunohistochemical study of microtubule -associated protein 2 and ubiquitinin chronically aluminum-intoxicated rabbit brain.
Takeda M. ± Tatebayashi Y. ± Tanimukai S. ± Nakamura Y. ± Tanaka T. ±
Nishimura T.
From: Acta Neuropathol (Berl) (1991) 82(5):346-52
Experimental neurofibrillary change was produced in rabbit brain by daily
subcutaneous aluminum tartrate injection for 40 days.
Neurotoxic effects of aluminium on embryonic chick brain cultures.
From: Acta Neuropathol (Berl) (1994) 88(4):359-66
Toxic damage of brain cells by aluminium (Al) is discussed as a possiblefactor in the development of neurodegenerative disorders in humans. Effec tsof Al on cell viability (lysosomal and mitochondrial activity) and differentiation(synthesis of cell-specific proteins) were found to the brain area specific withthe highest sensitivity observed in optic tectum.
Aluminium in tooth pastes and Alzheimer's disease.
The role of aluminium from tooth pastes may be even more important than thatfrom the drinking water.
Persistent subcutaneous nodules in chil dren hyposensitized with aluminium-containing allergen extracts.
Frost L. ± Johansen P. ± Pedersen S. ± Veien N. ± Ostergaard P.A. ± NielsenM.H.
From: Allergy (1985 Jul) 40(5):368-72
A follow-up study of 202 children who had received hyposensitizatio n with
aluminium-containingallergens showed that 1 -3 years after cessation of hyposensitization 13 children still had severely treatment -resistant
subcutaneous nodules in their forearms. Because of their long persistence thenodules of six children were studied in detail. Histologically, the nodules
showed infiltration with lymphocytes (forming germinal centres),
macrophages, plasma cells, mast cells and a few eosinophils.
In five patients aluminium crystals were found scattered between the cells and,in addition, the phagosomes of the macrophages contained aluminium. Patchtests for aluminium were positive in four of the six patients.
Contact sensitivity to aluminium in a patient hyposensitized with aluminium
precipitated grass pollen.
Clemmensen O. ± Knudsen H.E.
From: Contact Dermatitis (1980 Aug) 6(5):305 -8
Standard patch testing of a patient with eczema revealed positive reactions tothe aluminium discs used for testing.
Behavioural effects of gestational exposure to aluminium.
Rankin J. ± Sedowofia K. ± Clayton R. ± Manning A.
From: Ann Ist Super Sanita (1993) 29(1):147-52
The involvement of aluminium in the aetiology of a number of humanpathological diseases has altered its status from being a nontoxic,nonabsorbable, harmless element. This maybe of particular concern to thedeveloping foetus which is more susceptible to agents and at lower levels thanthe adult. Little attention has been given to aluminium's potential reproductivetoxicity until recently and further resear ch is required for a full evaluation of its
toxicity. Our preliminary results demonstrate behavioural and neurochemicalalterations in the offspring of mice exposed to aluminium during gestation.
Further, the effects of such exposure are also present in th e adult animalsuggesting persistent changes in behaviour following prenatal exposure.
The absence of extracellular calcium potentiates the killing of culturedhepatocytes by aluminum maltolate.
Snyder J.W. ± Serroni A. ± Savory J. ± Farber J.L.
From: Arch Biochem Biophys (1995 Jan 10) 316(1):434 -42
This data defines a new model in which aluminum kills liver cells by amechanisms distinct from previously recognized pathways of lethal cell injury.
It is hypothesized that aluminum binds to cytoskeleta l proteins intimatelyassociated with the plasma membrane. This interaction eventually disrupts the
permeability barrier function of the cell membrane, an event that heralds thedeath of the hepatocyte.
Sensitization to aluminium by aluminium -precipitated dust and pollen extracts.
Castelain P.Y. ± Castelain M. ± Vervloet D. ± Garbe L. ± Mallet B.
From: Contact Dermatitis (1988 Jul) 19(1):58 -60
... the means of sensitization was the inoculation of aluminium -precipitated
pollen or dust extracts for hyposensitization. We conclude that aluminiumallergy is not exceptional.
Allergy to non-toxoid constituents of vaccines and implications for patchtesting.
Cox N.H. ± Moss C. ± Forsyth A.
From: Contact Dermatitis (1988 Mar) 18(3):143 -6
Aluminium allergy causes false positive patch test reactions and we proposemethods of patch testing patients with symptoms at vaccination sites in order to avoid this problem.
Aluminium allergy in patients hyposensitized with aluminium -precipitatedantigen extracts.
Lopez S. ± Pelaez A. ± Navarro L.A. ± Montesinos E. ± Morales C. ± Carda C.
Aluminum precipitated antigen solutions, a small percentage of patientsdevelop persistent subcutaneous nodules at the injection site; the existence of
delayed sensitivity to aluminium has been implicated in the pathogenesis of these nodules.
Aluminium allergy.
Veien N.K. ± Hattel T. ± Justesen O. ± Norholm A.
From: Contact Dermatitis (1986 Nov) 15(5):295 -7
13 children ranging in age from 1 to 13 years and 1 adult patient had positive
patch tests to 2% AlCl3 in water. 13 of them had pruritic excoriated papules, 9at sites of hyposensitization therapy with aluminium -bound pollen extracts,
and 4 at sites of childhood immunization with an aluminium -bound vaccine(Di-Te-Pol).
Vaccination granulomas and aluminium allergy: course and prognostic
factors.
Kaaber K. ± Nielsen A.O. ± Veien N.K.
From: Contact Dermatitis (1992 May) 26(5):304 -6
21 children who had cutaneous granulomas following immunization with avaccine containing aluminium hydroxide, and who had positive patch tests to
aqueous aluminium chloride and/or to a Finn Chamber, were followed for 1 to8 years. During the period of observation, the symptoms cleared in 5 chil dren,
improved in 11, and remained unchanged in 5.
Short-term experimental acidification of a Welsh stream: toxicity of differentforms of aluminium at low pH to fish and invertebrates.
McCahon C.P. ± Pascoe D.
From: Arch Environ Contam Toxicol (1989 Jan-Apr) 18(1-2):233-42
Minimal effects were observed in the control and acid zones whilst largemortalities and reduced feeding were recorded in the acid and aluminiumzone.
H Differentiated neuroblastoma cells are more susceptible to aluminiumtoxicity than developing cells.
Pendlebury W.W. Perl D.P. Schwentker A. Pingree T.M. Solomon P.R.
From: Behav Neurosci (1988 Oct) 102(5):615-20
Aluminum intoxicated rabbits, in contrast, did not acquire the conditionedresponse over the 4 days of testing. This disruption of conditioning inaluminum-treated rabbits could not be attributed to deficits in sensory or
motor processes or to illness. Neuropathological analysis revealedwidespread neurofibrillary tangle formation in aluminum-treated animals.
Aluminum, a neurotoxin which affects diverse metabolic reactions.
Joshi J.G.
From: Biofactors (1990 Jul) 2(3):163-9
Experimental evidence is summarized to support the hypothesis that chronicexposure to low levels of aluminum may lead to neurological disorders.
Distribution of aluminum in different brain regions and body organs of rat.
From: Biol Trace Elem Res (1996 May) 52(2):181 -92
In the present study, an attempt has been made to investigate the distributionof aluminum in different regions of brain and body organs of male albino rats,
following subacute and acute aluminum exposure. Aluminum was observed toaccumulate in all regions of the brain with maximum accumulation in the
hippocampus. Aluminum was also seen to compartmentalize in almost all thetissues of the body to varying extents, and the highest accumu lation was inthe spleen.
Ti-6Al-4V ion solution inhibition of osteogenic cell phenotype as a function of differentiation timecourse in vitro.
Thompson G.J. ± Puleo D.A.
From: Biomaterials (1996 Oct) 17(20):1949-54
These results indicate that ions associated with Ti-6Al-4V alloy inhibited thenormal differentiation of bone marrow stromal cells to mature osteoblasts invitro, suggesting that ions released from implants in vivo may contribute toimplant failure by impairing normal bone deposition.
Aluminium release from glass ionomer cements during early water exposure invitro.
Andersson O.H. ± Dahl J.E.
From: Biomaterials (1994 Sep) 15(11):882-8
Aluminium is a major constituent of glass ionomer cements. During mixingand setting aluminium is released from the glass into the polyalkeonic acidsolution. Part of this aluminium may not combine with the polyalkeonic acid,but may be released from the cement. The aluminium release from auto -cured
and light-cured glass ionomer cements during early wa ter exposure wasstudied. The former cements released more aluminium than the latter. It is
suggested that the considerable release of aluminium from glass ionomer cements during early water exposure may explain the reported lack of
mineralization of predentin in the pulp beneath glass ionomer cements. Thiswould correspond to the inhibiting effect of aluminium on bone mineralization.
Impaired control of information transfer at an isolated synapse treated byaluminum: is it related to dementia?
These results indicate that aluminum at concentrations similar to those foundin the diseased brain of demented patients modulates synaptic transmission.
Chronic aluminum-induced motor neuron degeneration: clinical,neuropathological and molecular biological aspects.
Strong M.J. ± Garruto R.M.
From: Can J Neurol Sci (1991 Aug) 18(3 Suppl):428 -31
Aluminum chloride induces aggregates of phosphorylated neurofilament thatmimics the intraneuronal inclusions of amyotrophic lateral sclerosis.
Some commonly unrecognized manifestations of metabolic arthropathies.
Cobby M.J. ± Martel W.
From: Clin Imaging (1992 Jan-Mar) 16(1):1-14
The metabolic arthropathies are characterized by the deposit ion of abnormalsubstances in or around joints. Certain features of some of thesearthropathies and their significance have only recently been recognized and
others have been insufficiently emphasized. An important group of conditionsare the arthropathies related to renal failure and its treatment, namely,
aluminum toxicity, periarticular calcification and crystal deposition,hyperparathyroidism, and dialysis-related amyloidosis. Crystal deposition
diseases, specifically, gouty arthritis, calcium pyrophosp hate deposition, and
calcium hydroxyapatite deposition, are also reviewed.
Sepsis: a cause of aluminum release from tissue stores associated with acuteneurological dysfunction and mortality.
Davenport A. ± Williams P.S. ± Roberts N.B. ± Bone J.M.
From: Clin Nephrol (1988 Jul) 30(1):48-51
We report six cases of patients with renal failure and exposure to aluminumwho developed septicemia. In all cases the serum aluminum increased
markedly. This may have contributed to the neurological dysfunction seen infive, and the deaths of four of the patients. We suggest that the rise in serumaluminum was due to the release of tissue -bound aluminum, resulting in anincrease in free, diffusable aluminum and that this jeopardized bothneurological function an d immunocompetence.
Daily intakes of aluminium were estimated for 14 age -sex groups based on theFood and Drug Administration's (FDA) Total Diet Study dietary exposure
model. Estimates of aluminium intakes ranged from 0.7 mg/day for 6 -11-month-old infants to 11.5 mg/day for 14 -16-year-old males. Average intakes for adult men and women were 8-9 and 7 mg/day, respectively. The major contributors to daily intake of aluminium were foods with aluminium -containing food additives, e.g. grain products and processed cheese.
Transverse fractures of the spinous process of the 7th cervical vertebra inRDT patients: an Al related disease?
From: Int J Artif Organs (1987 Mar) 10(2):93-6
The bone fractures had occurred suddenly while the patients were going abouttheir daily work. These observations indicate that Al - or iron- related bonedisease with secondary hyperparathyroidism can i nduce bone fracture by onlyslight stress in patients maintained on hemodialysis.
Risk of aluminum accumulation in patients with burns and ways to reduce it.
Klein G.L. ± Herndon D.N. ± Rutan T.C. ± Barnett J.R. ± Miller N.L. ± Alfrey A.C.
From: J Burn Care Rehabil (1994 Jul-Aug) 15(4):354-8
Severely burned patients experience a bone lesion consisting of markedlyreduced bone formation and evidence of decreased resportion. The cause of the lesion may be multifactorial, but aluminum loading, which al so occurs inpatients with burns, has been documented to produce this type of injury inboth humans and animals.
Cutaneous exposure to aluminum is greatest from baths, which may provide
up to 8 mg aluminum. However, the dynamics of aluminum entry into the bloodvia a damaged skin barrier are unclear. Enteral exposure to aluminum is no
greater than daily dietary exposure. Parenteral sources of aluminum,especially 25% human serum albumin and calcium gluconate, provide the
most significant risk of loading be cause of direct introduction of aluminuminto the circulation.
Substitution with a different brand of albumin and calcium chloride can reduce
the parenteral aluminum load by as much as 95% and minimize any rolealuminum may play in the pathogenesis of this bone lesion.
Aluminum concentrations in tissues of rats: effect of soft drink packaging.
CT Aluminum in acidic surface waters: chemistry, transport, and effects.
From: Environ Health Perspect (1985 Nov) 63:93 -104
Ecologically significant concentrations of Al have been reported in surface
waters draining "acid-sensitive" watersheds that are receiving elevated inputsof acidic deposition. It has been hypothesized that mineral acids fromatmospheric deposition have re mobilized Al previously precipitated within thesoil during soil development. This Al is then thought to be transported toadjacent surface waters. Dissolved mononuclear Al occurs as aquo Al, as wellas OH-, F-, SO4(2-), and organic complexes.
Although past investigations have often ignored non-hydroxide complexes of
Al, it appears that organic and F complexes are the predominant forms of Al indilute (low ionic strength) acidic surface waters. The concentration of
inorganic forms of Al increases exponenti ally with decreases in solution pH.This response is similar to the theoretical pH dependent solubility of Al
mineral phases.
The concentration of organic forms of Al, however, is strongly correlated withvariations in organic carbon concentration of surf ace waters rather than pH.Elevated concentrations of Al in dilute acidic waters are of interest because: Alis an important pH buffer; Al may influence the cycling of important elementslike P, organic carbon, and trace metals; and Al is potentially toxic to aquatic
In carp exposed to pH 5.2 in fresh water, the Ca2+ influx from the water isreduced by 31% when compared to fish in water of neutral pH. At pH 5.2, the
Ca2+ influx but not Na+ uptake is decreased by aluminum (Al). Al reducesCa2+ influx dose-dependently: a maximum 55% reduction was observed after
1-2 h exposure to 200 micrograms .1( -1) (7.4 microM) Al.
A mechanism for acute aluminium toxicity in fish
Exley C. ± Chappell J.S. ± Birchall J.D.
From: J Theor Biol (1991 Aug 7) 151(3):417-28
Aluminium is acutely toxic to fish in acid waters. The gill is the principal targetorgan and death is due to a combination of ionoregulatory, osmoregulatory
and respiratory dysfunction. The mechanism of epithelial cell death isproposed as a general mechanism of aluminium -induced accelerated cell
death.
Can the mechanisms of aluminum neurotoxicity be integrated into a unifiedscheme?
From: J Toxicol Environ Health (1996 Aug 30) 48(6):599 -613
Regardless of the host, the route of administration, or the speciation,
aluminum is a potent neurotoxicant. In the young adult or developmentallymature host, the neuronal response to Al exposure can be dichotomized on
morphological grounds. In one, intraneuronal neurofilamentous aggregatesare formed, whereas in the other, significant neurochemical and
neurophysiological perturbations are induced wi thout neurofilamentousaggregate formation.
Evidence is presented that the induction of neurofilamentous aggregates is aconsequence of alterations in the posttranslational processing of neurofilament (NF), particularly with regard to phosphorylation stat e. AlthoughAl has been reported to impact on gene expression, this does not appear to be
critical to the induction of cytoskeletal pathology.
In hosts responding to Al exposure without the induction of cytoskeletalpathology, impairments in glucose utilization, agonist -stimulated inositol
phosphate accumulation, free radical -mediated cytotoxicity, lipid peroxidation,reduced cholinergic function, and altered protein phosphorylation have been
described. The extent to which these neurochemical modifications correlatewith the induction of a characteristic neurobehavioral state is unknown.
In addition to these paradigms, Al is toxic in the immediate postnatal interval.Whether unique mechanisms of toxicity are involved during developmentremains to be determined. In this article, the mechanisms of Al neurotoxicityare reviewed and recommendations are put forth with regard to futureresearch.
Mental status changes in an immunosuppressed child can be due to a varietyof causes; aluminum toxicity is rarely considered. We report a teenage girlwith acute lymphoblastic leukemia who developed mental status changes,speech disturbance, coarse tre mor, and abnormal EEG findings following
intravesical 1% alum irrigation and administration of aluminum -containingantacids. All abnormalities resolved after a nine -week course of intravenous
deferoxamine.
Progressing encephalomyelopathy with muscular a trophy, induced by
aluminum powder.
Bugiani O. ± Ghetti B.
From: Neurobiol Aging (1982 Fall) 3(3):209 -22
The injection of aluminum powder into the cerebrospinal fluid of adult rabbitsinduced a slowly progressing encephalomyelopathy characterized at first byalteration of posture and then by myoclonic jerks and muscle weakness.